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Chmelar, J.* ; Chatzigeorgiou, A.* ; Chung, K.-J. ; Prucnal, M.* ; Voehringer, D.* ; Roers, A.* ; Chavakis, T.

No role for mast cells in obesity-related metabolic dysregulation.

Front. Immunol. 7:524 (2016)
Verlagsversion DOI
Open Access Gold
Creative Commons Lizenzvertrag
Obesity-related adipose tissue (AT) inflammation that promotes metabolic dysregulation is associated with increased AT mast cell numbers. Mast cells are potent inducers of inflammatory responses and could potentially contribute to obesity-induced AT inflammation and metabolic dysregulation. Conflicting findings were reported on obesity-related metabolic dysfunction in mast cell-deficient mice, thus creating a controversy that has not been resolved to date. Whereas traditional Kit hypomorphic mast cell-deficient strains featured reduced diet-induced obesity and diabetes, a Kit-independent model of mast cell deficiency, Cpa3(Cre/+) mice, displayed no alterations in obesity and insulin sensitivity. Herein, we analyzed diet-induced obesity in Mcpt5-Cre R-DTA mice, in which the lack of mast cells is caused by a principle different from mast cell deficiency in Cpa3(Cre/+) mice or Kit mutations. We observed no difference between mast cell-deficient and -proficient mice in diet-induced obesity with regards to weight gain, glucose tolerance, insulin resistance, metabolic parameters, hepatic steatosis, and AT or liver inflammation. We conclude that mast cells play no essential role in obesity and related pathologies.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Mast Cell Deficiency ; Diet-induced Obesity ; Metabolic Dysregulation ; Insulin Resistance ; Glucose Tolerance; Adipose-tissue Inflammation; Insulin-resistance; Protects Mice; Deficiency; Disease; Fat; Ige; Costimulation; Macrophages; Pathogens
Sprache englisch
Veröffentlichungsjahr 2016
HGF-Berichtsjahr 2016
ISSN (print) / ISBN 1664-3224
e-ISSN 1664-3224
Quellenangaben Band: 7, Heft: , Seiten: , Artikelnummer: 524 Supplement: ,
Verlag Frontiers
Verlagsort Lausanne
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Pancreatic Islet Research (IPI)
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502600-001
Erfassungsdatum 2016-12-23